Editor's Comment: In this study, the researchers implicated a peptide named Diazepam Binding Inhibitor (DBI) as a source of fatigue in patients receiving androgen deprivation therapy for prostate cancer, and in patients with ME/CFS. DBI is a natural GABA-A inverse agonist, that is, it produces the opposite effects of anxiolytics (e.g. Valium). Subjects injected with synthetic DBI experience sweating, nausea, palpitations, tightness in the chest, restlessness and generalized anxiety. Certain steroids, among which is DHEA, the precursor to estrogen, bind to GABA-A receptors, producing effects similar to anxiolytics. Other hormones, such as pregnenolone, the precursor to progesterone, have effects similar to DBI. The implication of this study for ME/CFS patients is that increased DBI not only is related to heightened anxiety states (i.e. upregulated sympathetic activity), but to fatigue as well.

CONCLUSIONS: PCF patients differed from controls and CFS in mean expression of 10 genes from all 5 pathways. Correlations with fatigue severity implicated DBI for both patient groups and P2RY1 for PCF only. These pathways may provide new targets for interventions to reduce fatigue.

Thanks indeed for the editor's commentary preceding the introduction to this paper. Not surprisingly, understanding a condition as central to core metabolism as CFS/ME seems to be is going to require integrating detailed knowledge across a broad spectrum of scientific disciplines--and their related jargons. As my father was wont to say, "It's tough telling the players without a scorecard."